% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{AlfonsoGonzalez:276065,
      author       = {C. Alfonso-Gonzalez and I. Legnini and S. Holec and L.
                      Arrigoni and H. C. Ozbulut and F. Mateos and D. Koppstein
                      and A. Rybak-Wolf and U. Bönisch and N. Rajewsky$^*$ and V.
                      Hilgers},
      title        = {{S}ites of transcription initiation drive m{RNA} isoform
                      selection.},
      journal      = {Cell},
      volume       = {186},
      number       = {11},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-00971},
      pages        = {2438-2455.e22},
      year         = {2023},
      note         = {2023 May 25;186(11):2438-2455.e22},
      abstract     = {The generation of distinct messenger RNA isoforms through
                      alternative RNA processing modulates the expression and
                      function of genes, often in a cell-type-specific manner.
                      Here, we assess the regulatory relationships between
                      transcription initiation, alternative splicing, and 3' end
                      site selection. Applying long-read sequencing to accurately
                      represent even the longest transcripts from end to end, we
                      quantify mRNA isoforms in Drosophila tissues, including the
                      transcriptionally complex nervous system. We find that in
                      Drosophila heads, as well as in human cerebral organoids, 3'
                      end site choice is globally influenced by the site of
                      transcription initiation (TSS). 'Dominant promoters,'
                      characterized by specific epigenetic signatures including
                      p300/CBP binding, impose a transcriptional constraint to
                      define splice and polyadenylation variants. In vivo
                      deletion or overexpression of dominant promoters as well as
                      p300/CBP loss disrupted the 3' end expression landscape. Our
                      study demonstrates the crucial impact of TSS choice on the
                      regulation of transcript diversity and tissue identity.},
      keywords     = {5ʹ-3ʹ coupling (Other) / Drosophila (Other) / alternative
                      polyadenylation (Other) / human brain organoids (Other) /
                      long-read sequencing (Other) / mRNA isoform (Other) /
                      nervous system (Other) / p300/CBP (Other) / transcription
                      (Other) / transcription start site (Other)},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37178687},
      doi          = {10.1016/j.cell.2023.04.012},
      url          = {https://inrepo02.dkfz.de/record/276065},
}